Reconstituted High Density Lipoprotein Modulates Adherence of Polymorphonuclear Leukocytes to Human Endothelial Cells

Moudry, R; Mo, Spycher; Je, Doran

doi:10.1097/00024382-199703000-00004

Cited by 49 publications

(33 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Some HDL preparations can inhibit integrin and adhesion molecule expression in leukocytes and ECs and reduce their adhesive interaction. 26,27 Our current data suggest that one property of "antiinflammatory" HDL may be reduced apoCIII content. Inhibition of adhesion by HDL apoCIII Ϫ was more prominent under static than shear flow conditions.…”

Section: Discussionmentioning

confidence: 69%

Apolipoprotein CIII in Apolipoprotein B Lipoproteins Enhances the Adhesion of Human Monocytic Cells to Endothelial Cells

et al. 2006

View full text Add to dashboard Cite

Background-Lipoproteins containing apolipoprotein (apo) CIII predict coronary heart disease and associate with components of the metabolic syndrome. ApoCIII inhibits lipoprotein catabolism in plasma. However, it is unknown whether apoCIII itself, or in association with VLDL, LDL, or HDL, directly affects atherogenic mechanisms in vascular cells. Thus, we investigated the direct effect of lipoproteins that do or do not have apoCIII, and apoCIII itself, on adhesion of THP-1 cells, a human monocytic cell line, to vascular endothelial cells (ECs). Methods and Results-VLDL CIIIϩ and LDL CIII ϩ (100 g apoB/mL) from fasting plasma of 18 normolipidemic volunteers increased THP-1 cell adhesion to ECs under static conditions by 2.4Ϯ0.3-fold and 1.8Ϯ0.7-fold, respectively (PϽ0.01), whereas VLDL or LDL without apoCIII did not affect THP-1 cell adhesion. ApoCIII (100 g/mL), but not apoCI, apoCII or apoE, also increased THP-1 cell adhesion by 2.1Ϯ0.6-fold. Studies with human peripheral blood monocytes yielded similar results. ApoCIII also had strong proadhesive effects under shear flow conditions. VLDL CIII ϩ , LDL CIII ϩ , or apoCIII itself activated PKC␣ and RhoA in THP-1 cells, which resulted in ␤1-integrin activation and enhancement of THP-1 cell adhesion. Interestingly, HDL CIII ϩ did not affect THP-1 cell adhesion, whereas HDL without apoCIII decreased their adhesion. Conclusions-ApoB lipoproteins that contain apoCIII increase THP-1 cell adhesion to ECs via PKC␣ and RhoA-mediated ␤1-integrin activation. These results indicate that apoCIII not only modulates lipoprotein metabolism but also may directly contribute to the development of atherosclerosis. (Circulation. 2006;113:691-700.)

show abstract

Section: Discussionmentioning

confidence: 69%

Apolipoprotein CIII in Apolipoprotein B Lipoproteins Enhances the Adhesion of Human Monocytic Cells to Endothelial Cells

et al. 2006

View full text Add to dashboard Cite

show abstract

“…By blocking lipopolysaccharide activity and decreasing CD11b/CD18 upregulation, rHDL has also been shown to decrease lipopolysaccharide-induced adhesion of leukocytes to human endothelial cells (53). In addition, the anti-oxidative activity of HDL is typically characterized by its ability to inhibit LDL oxidation (54) but it has also been shown to inhibit the formation of reactive oxygen species (55,56).…”

Section: Other Potentially Atheroprotective Propertiesmentioning

confidence: 99%

The HDL hypothesis: does high-density lipoprotein protect from atherosclerosis?

Vergeer

Holleboom

Kastelein

et al. 2010

Journal of Lipid Research

200

122

View full text Add to dashboard Cite

This article is available online at http://www.jlr.org the imagination. Because of a general consensus that HDL protects against atherosclerosis, what we shall term the HDL hypothesis, strategies have been developed to raise plasma HDL levels or to improve HDL function. However, it is increasingly questioned whether such interventions will indeed reduce the risk of atherosclerosis. This review summarizes the reported evidence that supports the HDL hypothesis. EPIDEMIOLOGYA low plasma HDL-C concentration is among the strongest, statistically independent risk factors for cardiovascular disease (CVD) (2). In a widely cited meta-analysis of four large studies (total number of individuals studied: 15,252), a 1 mg/dl increase of HDL-C levels was reported to be associated with a 2-3% decreased CVD risk (3). This result provides an epidemiological argument in favor of therapeutically raising HDL-C levels. One may draw parallels with the detrimental consequences of elevated lowdensity lipoprotein cholesterol (LDL-C) levels and blood pressure, which have been successfully controlled through therapy, resulting in signifi cant reductions of cardiovascular mortality and morbidity (4, 5) . It should be noted, however, that the associations between elevated LDL-C and blood pressure and increased CVD risk refl ect causal relationships, whereas such a relation between low HDL-C levels and increased CVD is not undisputed (6, 7). This is related to the fact that HDL-C levels are infl uenced by many different variables that also affect CVD risk: 1 ) Men have on average lower HDL-C levels than women (8). (1) reported that plasma levels of high-density lipoprotein cholesterol (HDL-C) were reduced in patients with coronary artery disease. In 1977, Gordon et al. (2) subsequently showed that low HDL-C is a risk factor for coronary heart disease in the Framingham study. These important fi ndings have given rise to a large number of diverse HDL studies over the last few decades. The numerous different and apparently unrelated beneficial effects that have since been ascribed to HDL appeal to

show abstract

“…Furthermore, it is demonstrated that LPS stimulation evokes an increase in the expression of adhesion molecules, including L-selectin [7] and CD11b/CD18 in leukocytes, E-selectin and intercellular adhesion molecule 1 (ICAM-1) in endothelial cells [7][8][9][10][11][12][13] . In addition, LPS stimulation can cause the release of proinflammatory mediators and vasoactive substances, such Abstract AIM: To investigate the effect of compound Danshen injection on lipopolysaccharide (LPS)-induced rat mesenteric microcirculatory dysfunctions and the underlying possible mechanism by an inverted intravital microscope and high-speed video camera system.…”

Section: Introductionmentioning

confidence: 99%

Compound Danshen injection improves endotoxin-induced microcirculatory disturbance in rat mesentery

Han

Horie²,

Miura³

et al. 2007

WJG

View full text Add to dashboard Cite

stained with Monastral blue B, rolling and adhesion of leukocytes, production of oxygen radical in venular wall, albumin efflux and enhanced mast cell degranulation in vivo , all of which, except for the leukocyte rolling, were attenuated by the treatment with compound Danshen injection. Experiments performed in vitro further revealed that the expression of CD11b/CD18 and the production of oxygen free radical in neutrophils, and the expression of ICAM-1 in HUVECs were increased by exposure to LPS, and they were attenuated by compound Danshen injection. CONCLUSION: These results suggest that compoundDanshen injection is an efficient drug with multi-targeting potential for improving the microcirculatory disturbance. INTRODUCTIONIt is now well-recognized that stimulation with lipopolysaccharide (LPS) leads to a number of responses in microcirculation, such as endothelial cell damage, an increase in rolling, adhesion and emigration of leukocytes in post-capillary venules, enhanced oxygenfree radical production, mast cell degranulation and protein efflux [1][2][3][4][5][6] . Furthermore, it is demonstrated that LPS stimulation evokes an increase in the expression of adhesion molecules, including L-selectin [7] and CD11b/CD18 in leukocytes, E-selectin and intercellular adhesion molecule 1 (ICAM-1) in endothelial cells [7][8][9][10][11][12][13] . In addition, LPS stimulation can cause the release of proinflammatory mediators and vasoactive substances, such Abstract AIM: To investigate the effect of compound Danshen injection on lipopolysaccharide (LPS)-induced rat mesenteric microcirculatory dysfunctions and the underlying possible mechanism by an inverted intravital microscope and high-speed video camera system. METHODS:LPS was continuously infused through the jugular artery of male Wistar rats at the dose of 2 mg/kg per hour. Changes in mesenteric microcirculation, such as diameters of arterioles and venules, velocity of RBCs in venules, leukocyte rolling, adhesion and emigration, free radicals released from post-capillary venules, FITCalbumin leakage and mast cell degranulation, were observed through an inverted intravital microscope assisted with CCD camera and SIT camera. Meanwhile, the expression of adhesion molecules CD11b/CD18 and the production of free radical in neutrophils, and the expression of intercellular adhesion molecule 1 (ICAM-1) in human umbilical vein endothelial cells (HUVECs) were quantified by flow cytometry (FACS) in vitro . RESULTS:The continuous infusion with LPS resulted in a number of responses in microcirculation, including a significant increase in the positive region of venule

show abstract

Reconstituted High Density Lipoprotein Modulates Adherence of Polymorphonuclear Leukocytes to Human Endothelial Cells

Cited by 49 publications

References 0 publications

Apolipoprotein CIII in Apolipoprotein B Lipoproteins Enhances the Adhesion of Human Monocytic Cells to Endothelial Cells

Apolipoprotein CIII in Apolipoprotein B Lipoproteins Enhances the Adhesion of Human Monocytic Cells to Endothelial Cells

The HDL hypothesis: does high-density lipoprotein protect from atherosclerosis?

Compound Danshen injection improves endotoxin-induced microcirculatory disturbance in rat mesentery

Contact Info

Product

Resources

About